Mammalian oocyte quality degrades over time after in vitro ovulation. As various oocyte manipulations employed in assisted reproductive technology are time consuming, post-ovulatory aging is a serious problem in reproductive medicine and ova research. Shimoi et al. investigated the effects of post-ovulatory aging on the incidence of chromosomal aneuploidy during meiosis II (MII), with a focus on the expression of functional proteins from the spindle assembly checkpoint (SAC) (Shimoi G et al.: Destabilization of spindle assembly checkpoint causes aneuploidy during meiosis II in murine post-ovulatory aged oocytes. pp. 57–66). This study showed that post-ovulatory oocyte aging inhibits MAD2 localization to the sister kinetochore. Furthermore, oocyte aging prevented cohesin subunits from being appropriately maintained or degraded. These results suggest that destabilization of SAC signaling causes sister chromatid segregation errors in MII oocytes and consequently increases the incidence of aneuploidy in early embryos.